International Journal of

Environmental Research
and Public Health

Article
Canonical Correlation between
Behavioral-Psychological Variables and Predictors of
Coronary Artery Disease Prognosis
Chul-Hoon Kim 1 , In-Kyoung Noh 2 , Jung Mi Ryu 3 , Eun Jung Bae 3,4 , Hoo Jeung Cho 3 and
Myoung Soo Kim 3, *
1 College of Medicine, Dong-A University, Busan 49201, Korea; bbp2000@hanmail.net
2 Department of Internal Medicine, Kosin University Gospel Hospital, Busan 49267, Korea;
ada10kr@naver.com
3 Department of Nursing, Pukyong National University, Busan 48513, Korea;
rewmis@naver.com (J.M.R.); ccu0401@naver.com (H.J.C.)
4 Department of Nursing, Dongnam Institute of Radiological & Medical Sciences, Busan 46033, Korea;
beaulife-@hanmail.net
* Correspondence: kanosa@pknu.ac.kr; Tel.: +82-51-629-5782




Received: 17 January 2020; Accepted: 28 February 2020; Published: 2 March 2020


Abstract: Metabolic syndrome (MetS) and severity of coronary artery disease (CAD) are considered
predictors of CAD prognosis. Unhealthy lifestyles and type-D personality are associated with MetS
and are potential causes of primary and secondary CAD. In this cross-sectional descriptive study, we
aimed to investigate the relationship between behavioral-psychological variables and predictors of
CAD prognosis. The behavioral-psychological variable set contained six lifestyle categories and two
type-D personality categories. Descriptive analyses, t-tests, analysis of variance, Pearson’s correlation,
and canonical correlation were used. The behavioral-psychological variable set was related to the
predictor set for CAD prognosis, with a significant canonical variate of 0.67 (45% overlapping variance).
Significant pairs of canonical variates indicated that poor physical activity and weight control (−0.77),
poor dietary habits (−0.78), alcohol consumption and cigarette smoking (−0.37), lack of sleep and rest
(−0.40), stress (−0.64) in the lifestyle set, higher negative affectivity (0.52), and social inhibition (0.71)
in the type-D personality set were associated with a high MetS score (0.59) and severity of CAD (0.91).
A combination of behavioral and psychological variables was found to be important in predicting the
prognosis of CAD; therefore, interventions aimed at preventing combinations of these variables may
be effective in improving CAD prognosis.

Keywords: coronary artery disease; lifestyle; metabolic syndrome; severity of illness index;
type-D personality

1. Introduction
Coronary artery disease (CAD) is the most common type of ischemic heart disease. This
progressive and recurrent disease may present with atherosclerotic or non-atherosclerotic coronary
arteries [1]. Ischemic heart disease occurs not only owing to sclerosis of the coronary artery but
also due to functional coronary vasomotion, including vascular tone and coronary artery spasm [2].
Therefore, the management of CAD should involve improving the prognosis of patients with CAD
by modifying other detrimental factors and addressing issues arising within the diseased coronary
artery. Healthcare costs related to morbidity and mortality owing to CAD reportedly increase social
and economic burdens [3]. However, the mortality rate 2–3 years following CAD onset has been
found to be similar to that of the general population [4]; therefore, healthcare providers need be

Int. J. Environ. Res. Public Health 2020, 17, 1608; doi:10.3390/ijerph17051608 www.mdpi.com/journal/ijerph
Int. J. Environ. Res. Public Health 2020, 17, 1608 2 of 14

able to provide patients with CAD and their families with appropriate prognostic information. One
prognostic predictor of CAD is metabolic syndrome (MetS). MetS components can create a state of
oxidative stress that is linked to ischemic heart disease [5,6] and that increases a patient’s risk for
primary CAD [7]. Furthermore, the presence of MetS in young patients with CAD has been found to
be an important predictor of six-year major cardiac events (hazard ratio 3.32) and repeated myocardial
infarction (hazard ratio 7.78) [8]. Angiographic severity of CAD is another predicting factor, which is
indicative of the recurrent development of coronary atherosclerosis [9]. The severity of physiological
stenosis has also been shown to have a significant association with the risk of clinical events and
provide better prognostic stratification [10].
Unhealthy behaviors have been associated with the prognosis of CAD [11]. Guidelines recommend
30 min of moderate-intensity physical activity five days a week; however, non-adherence to exercise
remains problematic [12] despite physical activity playing a critical role in the secondary prevention of
cardiovascular diseases [13]. Sedentary lifestyles, such as sitting for a total of 6–7 h/day and 3–4 h/day
of TV viewing, have been associated with increased cerebrovascular disease-related mortality [14].
Moreover, based on angiography reports, the most prevalent type of coronary obstruction is due to
abnormal lipid profiles [15], which are often related to unhealthy lifestyle behaviors such as cigarette
smoking and an increased consumption of fat and sugar [16]. In addition, both short and long sleep
durations have been independently associated with higher all-cause mortality [17]; therefore, behavior
modification needs to be implemented to help prevent poor prognoses for patients with CAD.
According to a systematic review concerning risk factors for CAD, individual psychological
factors have also been found to be associated with prognosis and health outcomes, including
re-hospitalization and mortality [18]. Psychological factors such as depression, anxiety, social
isolation, psychosocial distress, and a type-D personality [18], which are known risk factors for
cardiovascular disease [19], have been reported to increase the risk of developing CAD by 32.5% [20].
Depression, distress, and anxiety are factors that have been reported to contribute to heart failure [21]
and atrial fibrillation [6] through several mechanisms. Individuals with a type-D personality are
defined as those with a tendency toward higher stress and anger levels, often because of psychological
depression [22]. With respect to a type-D personality, psychophysiological and behavioral pathways
have been identified as two potential mechanisms affecting the development of heart disease [23].
The psychophysiological pathway could involve an elevated cortisol awakening response that was
mediated by the hypothalamic–pituitary–adrenal axis in patients with acute coronary syndrome and a
type-D personality [24]. The behavioral pathway may contribute to the development of CAD through
behavioral issues such as sedentary lifestyle [25] and an unhealthy diet [26]. Specifically, the combined
effect of these two pathways may increase the risk of a cardiovascular event, and behavioral issues
have been shown to lead to advanced complications of cardiovascular disease later in life [27].
Although several studies have demonstrated the role of behavioral-psychological factors on
CAD [28,29], empirical studies on predictors of CAD prognosis such as MetS and its relationship with the
severity of CAD are lacking, and their results are inconsistent [27,30]. Furthermore, the interconnections
of different behavioral-psychological factors with different MetS components and the severity of CAD
have not been investigated in detail. Type-D personality traits have been shown to be related to
maladaptive health-related behavior [31] and are associated with an increased severity of CAD [13];
therefore, assessing combinations of behavioral and psychological variables could be expected to
provide more extensive information than a bivariate relationship with MetS components and CAD
severity alone and may help refine guidelines for patients at a risk of CAD. Therefore, two research
questions were set: is there a relationship between behavioral-psychological variables and predictors
for CAD prognosis? If so, which combination is most strongly related to CAD prognosis?
Int. J. Environ. Res. Public Health 2020, 17, 1608 3 of 14

Int. J. Environ.
2. Materials andRes. Public Health 2020, 17, 1608
Methods 3 of 14

2. Materials
2.1. Study Designand
andMethods
Participants
This cross-sectional
2.1. Study descriptive study involved interviews using a structured survey and a review
Design and Participants
of medical records. Patients were recruited from a cardiology outpatient department at a tertiary
This cross-sectional descriptive study involved interviews using a structured survey and a
hospital
review of medical records. criteria
in Korea. Inclusion Patients comprised participants
were recruited diagnosed
from a cardiology with CAD
outpatient [stableatangina
department a
pectoris, unstable
tertiary angina
hospital pectoris,
in Korea. ST segment
Inclusion criteria -elevation
comprised myocardial infarction with
participants diagnosed (STEMI),
CADand non-ST
[stable
elevation
anginamyocardial infarction
pectoris, unstable (NSTEMI)]
angina based
pectoris, ST on coronary
segment angiography
-elevation myocardial results,
infarction those who
(STEMI), and had
non-ST elevation myocardial infarction (NSTEMI)] based on coronary angiography
not undergone a previous cardiac intervention, those with no cognitive function or communication results, those
who had and
impairments, not those
undergone
who aconsented
previous tocardiac intervention,
participation those
in this withExclusion
study. no cognitive function
criteria or
comprised
communication impairments, and those who consented to participation in this study.
participants with incomplete information in their medical records and those who declined to undertake Exclusion
criteria comprised participants with incomplete information in their medical records and those who
an interview. Figure 1 shows the flowchart of the study population. The required sample size in a
declined to undertake an interview. Figure 1 shows the flowchart of the study population. The
canonical correlation is 10 times per variable [32]. This study comprised 108 participants, which was
required sample size in a canonical correlation is 10 times per variable [32]. This study comprised
sufficient for the analysis of 10 variables (six variables for behavior components, two variables for
108 participants, which was sufficient for the analysis of 10 variables (six variables for behavior
type-D personality,
components, twoand two predictive
variables for type-Dvariables forand
personality, CADtwoprognosis).
predictive variables for CAD prognosis).

Participants admitted
with cardiac symptoms (n=248)

Excluded:
-Not diagnosed with CAD (n=27)
-Experience of a previous cardiac intervention (n=92)
-Cognitive function or communication impairment (n=2)
-Decline to participation (n=15)

Review of medical records (n=112)

Excluded:
-Incomplete information in medical records (n=3)
-Decline to undertake an interview (n=1)

Participants included in the

analysis (n=108)

Figure 1. Flowchart
Figure 1. Flowchart of
of study
study population.
population.

2.2. Measurements
2.2. Measurements

2.2.1. 2.2.1.
Sociodemographic and
Sociodemographic Disease-Related
and Disease-RelatedCharacteristics
Characteristics
All participant characteristics
All participant characteristicswere
wereobtained
obtained at the time
at the timeofofdiagnosis
diagnosis from
from thethe survey
survey and and
the the
medical record
medical data.data.
record Sociodemographic
Sociodemographiccharacteristics includedthethe
characteristics included following
following six six items:
items: age, age,
sex, sex,
educational
educational status,
status, marital
marital status,
status, subjectiveeconomic
subjective economic status,
status,andandhealth
health status.
status.Subjective
Subjectiveeconomic
economic
statusstatus
and and health
health status
status werewere classifiedas
classified aslow
low (coded
(coded 1),1),moderate
moderate (coded
(coded 2), 2),
andand
highhigh(coded 3). 3).
(coded
Disease-related characteristics included the following six items: cigarette smoking
Disease-related characteristics included the following six items: cigarette smoking history, family history, family
history, type of CAD, and the use of antihypertensive, antidiabetic, and antihyperlipidemic
history, type of CAD, and the use of antihypertensive, antidiabetic, and antihyperlipidemic medication.
medication. Cigarette smoking history was classified as follows: non-smoker, past smoker, and
Cigarette smoking history was classified as follows: non-smoker, past smoker, and current smoker.
current smoker. Family history was assessed to determine whether there was a family history of
Family history was assessed to determine whether there was a family history of CAD. The type of CAD
CAD. The type of CAD was classified into two categories, namely angina pectoris, including stable
was classified into two
angina pectoris, andcategories, namely
acute coronary angina pectoris,
syndrome, including including
unstable stable
anginaangina
pectoris,pectoris,
STEMI,and andacute
coronary syndrome,
NSTEMI. The useincluding unstable
of medication angina pectoris,
was classified STEMI,
as either “yes” and1)NSTEMI.
(coded The use
or “no” (coded 0). of medication
was classified as either “yes” (coded 1) or “no” (coded 0).
Int. J. Environ. Res. Public Health 2020, 17, 1608 4 of 14

2.2.2. Behavioral-Psychological Variable Set

The behavioral-psychological variable set contained six variables in the lifestyle subcategory and
two variables in the type-D personality subcategory.

Lifestyle (Behavioral Set)

A lifestyle evaluation tool for patients with MetS [33] was used to assess participant lifestyle. This
36-item instrument comprised 6 dimensions, namely physical activity and weight control (8 items),
dietary habits (16 items), alcohol consumption and cigarette smoking (3 items), sleep and rest (2 items),
stress (3 items), and medication and health management (4 items). Item responses were measured
using a 4-point scale from 1 (not at all) to 4 (always). Higher scores corresponded to a healthy lifestyle.
Internal consistency in the original study reported a value of 0.92 [33], and this study had an internal
consistency value of 0.93.

Type-D Personality (Psychological Set)

We used “The Korean type-D scale-14” that was developed by Denollet [22] and verified in Korean
by Lim et al. [34]. This scale comprised two parts, namely negative affectivity and social inhibition, each
with 7 items. Assessments were based on a 5-point scale from 0 (definitely disagree) to 4 (definitely
agree). Cronbach’s alpha for negative affectivity and social inhibition were 0.88 and 0.86, respectively,
in the development study [22], and 0.83 and 0.82, respectively, in this study.

2.2.3. Predictors of CAD Prognosis Variable Set

The variable set for predictors of CAD prognosis contained two variables, namely the MetS score
and the severity of CAD.

MetS Score
To identify MetS, we used the National Cholesterol Education Program-Adult Treatment Panel III
(NCEP-ATP III) [35] for triglycerides, high-density lipoprotein-cholesterol (HDL-C), blood pressure,
and fasting glucose. To diagnose MetS, the NCEP-ATP III [35] requires the presence at least 3 of
the following components: (1) hypertriglyceridemia (triglycerides >150 mg/dL); (2) low HDL-C
(HDL-C < 40 mg/dL in men or <50 mg/dL in women); (3) hypertension (systolic blood pressure
>130 mmHg or diastolic blood pressure >85 mmHg); (4) hyperglycemia (fasting glucose concentration
>100 mg/dL or diagnosed with type 2 diabetes); and (5) abdominal obesity (waist circumference
>90 cm in men and >88 cm in women, for Asian populations). Furthermore, treatment with specific
medications, including medications used to manage blood pressure, triglycerides, cholesterol, and
glucose levels, should be considered. However, due to a lack of waist circumference data recorded over
the same period as the other four components, body mass index (BMI) >25 kg/m2 was used based on
the obesity criterion recommendations of the Korean Society for the Study of Obesity [36]. To calculate
the MetS score, each component was classified as yes (coded 1) or no (coded 0). The MetS score ranged
from 0 to 5, with a higher score indicating a greater severity MetS.

Severity of CAD
To determine the severity of CAD, we used the number of significantly stenotic coronary arteries
(including arterial branches), as noted in the medical records. Intravascular ultrasonography was
analyzed independently by a radiologist and a physician to characterize the extent and the degree of
stenosis. Significant stenosis was defined as > 50% occlusion of the coronary artery’s internal diameter.
No significant stenosis vs. significant stenosis was scored as 0 vs. 1; respectively, significant stenosis
in 1 vessel vs. 2 vessels vs. 3 vessels was scored as 1 vs. 2 vs. 3, respectively, with the highest score
indicating increased severity.
Int. J. Environ. Res. Public Health 2020, 17, 1608 5 of 14

2.3. Ethical Considerations

This study was conducted following a review and approval from the hospital’s Institutional
Review Board (IRB no. 1608012044). Prior to data collection, researchers met with the participants and
provided them with an information sheet explaining the study aims, the confidentiality of personal
information, the anonymity of the survey, and the voluntary nature of participation. Written consent
was obtained from participants prior to questionnaire distribution. This study complied ethically with
the Declaration of Helsinki.

2.4. Data Analysis

Statistical Package for the Social Science (SPSS) version 23.0 (SPSS Inc., Chicago, IL, USA) was
used to analyze the data. For descriptive analyses, a t-test or a Mann–Whitney U-test, an analysis of
variance or a Kruskal–Wallis test, and a Pearson’s correlation were used. Canonical correlation analysis
was performed after the assumptions of the canonical correlation were examined. Pairs of canonical
variates were interpreted as reliable if the structure coefficient was >0.30 because an explanatory power
> 9% was deemed to be a meaningful value [32].

3. Results

3.1. Predictors of CAD Prognosis According to Participant Characteristics

Table 1 shows the MetS score and the severity of CAD according to participant characteristics.
The mean age of the participants was 62.8 ± 10.5 years, and 51.9% of the participants were male. There
were no significant differences in MetS score; however, we observed a significant difference according
to subjective health status (F = 5.79, p = 0.004), antidiabetic medication use (t = −4.01, p < 0.001),
and antihyperlipidemic medication use (t = −3.18, p = 0.002). There were significant differences in
the severity of CAD according to age (H = 9.66, p = 0.022), type of CAD (Z = −2.99, p = 0.003), and
antihypertensive medication use (Z = −3.39, p = 0.001).

Table 1. Predictors of coronary artery disease (CAD) prognosis according to participant characteristics
(N = 108).

MetS Severity
Characteristics Categories N (%) t/F(p) Z/H(p)
Score of CAD
Age (years) 40–49 13 (12.0) 3.15 ± 1.46 0.21 0.54 ± 1.66 9.66
50–59 24 (22.2) 2.79 ± 1.53 (0.887) 1.13 ± 1.04 (0.022)
60–69 39 (36.1) 2.95 ± 1.34 1.41 ± 0.99
70≤ 32 (29.6) 2.88 ± 1.24 1.44 ± 0.98
Gender Male 56 (51.9) 2.93 ± 1.39 0.09 1.34 ± 0.98 −1.11
Female 52 (48.1) 2.90 ± 1.33 (0.925) 1.15 ± 1.02 (0.269)
Educational ≤Elementary 26 (24.1) 2.77 ± 1.31 0.32 1.50 ± 1.07 0.02
Status Middle 18 (16.7) 3.17 ± 1.51 (0.810) 1.44 ± 0.10 (0.880)
High 54 (50.0) 2.89 ± 1.34 1.09 ± 0.96
≥University 10 (9.3) 3.00 ± 1.41 1.10 ± 0.74
Marital status Single 3 (2.8) 4.33 ± 0.58 1.86 1.00 ± 0.01 −0.32
Married 105 (97.2) 2.88 ± 1.35 (0.066) 1.26 ± 1.01 (0.746)
Subjective Low 19 (17.6) 3.47 ± 1.39 2.01 1.63 ± 1.12 4.14
Economic Moderate 58 (53.7) 2.78 ± 1.26 (0.139) 1.28 ± 1.04 (0.126)
Status High 31 (28.7) 2.84 ± 1.46 0.97 ± 0.75
Subjective Good 26 (24.1) 2.42 ± 1.47 5.79 0.96 ± 0.99 4.28
Health Moderate 24 (22.2) 2.50 ± 1.18 (0.004) 1.13 ± 0.80 (0.118)
Int. J. Environ. Res. Public Health 2020, 17, 1608 6 of 14

Table 1. Cont.

MetS Severity
Characteristics Categories N (%) t/F(p) Z/H(p)
Score of CAD
Status Bad 58 (53.8) 3.31 ± 1.26 1.43 ± 1.05
Smoking Non-smoker 49 (45.4) 3.06 ± 1.35 0.51 1.29 ± 1.04 1.90
History Past smoker 26 (24.1) 2.81 ± 1.30 (0.603) 1.04 ± 0.99 (0.386)
Current smoker 33 (30.6) 2.79 ± 1.43 1.36 ± 0.93
Family Yes 90 (83.3) 2.94 ± 1.34 0.48 1.23 ± 0.96 −0.49
History No 18 (16.7) 2.78 ± 1.44 (0.636) 1.33 ± 1.03 (0.625)
Type of CAD Angina pectoris 22 (20.4) 2.86 ± 1.49 −0.21 0.68 ± 0.72 −2.99
Acute coronary 86 (79.6) 2.93 ± 1.33 (0.838) 1.40 ± 1.01 (0.003)
syndrome
Antihypertensive Yes 51 (47.2) 2.67 ± 1.37 −1.84 0.90 ± 0.83 −3.39
drug No 57 (52.8) 3.14 ± 1.32 (0.69) 1.56 ± 1.04 (0.001)
Antidiabetic Yes 79 (73.1) 2.62 ± 1.29 −4.01 1.20 ± 0.97 −0.72
drug No 29 (26.9) 3.72 ± 1.19 (<0.001) 1.38 ± 1.08 (0.470)
Antihyperlipidemic Yes 101 (93.5) 2.81 ± 1.32 −3.18 1.20 ± 0.98 −1.94
0
drug No 7 (6.5) 4.43 ± 0.79 (0.002) 2.00 ± 1.00
(0.052)
MS = metabolic syndrome.

3.2. Lifestyle, Type- D Personality, MetS Score, and Severity of CAD

The highest lifestyle factor scores were for stress, whereas physical activity and weight control
had the lowest lifestyle scores. The mean negative affectivity score was 3.43 ± 0.82, and the mean
social inhibition score was 2.71 ± 1.00. The mean MetS score was 2.92 ± 1.35, and the mean severity
score for CAD was 1.25 ± 0.99 (Table 2). Figure 2 shows the characteristics of the MetS score and
the severity of CAD. For the MetS component assessment, the prevalence rates for hypertension
and hypertriglyceridemia were 80.6% and 38.9%, respectively. The proportion of participants with
significant stenosis in the left anterior descending artery (LAD) was 50.9%. Approximately 40% of the
participants had significant stenosis in at least one vessel, and 14.8% had fixed stenosis in >50% of the
internal diameter in three coronary arteries.

Table 2. Descriptive statistics of behavioral-psychological variables and predictors of CAD prognosis

(N = 108).

Variables (Number of Items/Unit) Mean ± SD Actual Range Potential Range

Behavioral-psychological variables
Lifestyle (behavioral variables)
Physical activity and weight control (8) 1.87 ± 0.74 1.00~3.50 1.00~4.00
Dietary habit (16) 2.32 ± 0.50 1.44~3.25 1.00~4.00
Drinking and smoking (3) 2.79 ± 1.01 1.00~3.67 1.00~4.00
Sleep and rest (3) 1.93 ± 0.50 0.67~2.67 1.00~4.00
Stress (2) 3.69 ± 0.90 2.00~4.00 1.00~4.00
Drug and health management (4) 2.30 ± 0.72 1.00~3.75 1.00~4.00
Type-D personality (psychological variables)
Negative affectivity (7) 3.43 ± 0.82 0~4.00 0~4.00
Social inhibition (7) 2.71 ± 1.00 0~4.00 0~4.00
Int. J. Environ. Res. Public Health 2020, 17, 1608 7 of 14

Table 2. Cont.

Variables (Number of Items/Unit) Mean ± SD Actual Range Potential Range

Int. J. Environ. Predictors
Res. Public Health 2020,prognosis
for CAD 17, 1608 7 of 14

Metabolic syndrome score 2.92 ± 1.35 0~5.00 -

3.3. Correlation between the Behavioral-Psychological Variable Set and Predictors of CAD Prognosis
Triglyceride (mg/d L) 134.78 ± 71.17 38~428 -
Assumption tests were conducted before the canonical correlation analysis. The normality, the
HDL-cholesterol (mg/d L) 47.40 ± 14.38 28.0~94.6 -
linearity, and the homoscedasticity met the assumptions, except for MetS components and the
Systolic blood pressure (mmHg) ± 21.32
degree of stenosis in each artery. The correlation131.75between 60~190
behavioral-psychological -
variables and
Diastolic blood pressure (mmHg) 78.80 ± 12.51 30~110
predictors of CAD prognosis was between 0.20~0.42, which showed an absence of multicollinearity -
(Table 3). Glucose (mg/d L) 116.27 ± 39.27 69~244 -
The behavioral-psychological
BMI (kg/m )2 variable set was related
25.25 ± 2.90to the predictor
18.2~32.0 set of CAD - prognosis
with one significant canonical variate of 0.67 (45% overlapping variance) (Table 4). Wilk’s Lambda
Severity of coronary artery disease (%) 1.25 ± 0.99 0~3.00 0~3.00
value with all canonical correlations was 0.51, which was statistically significant (F = 4.91, p < 0.001).
Degree of left anterior descending artery stenosis 48.58 ± 36.83 0~100 0~100
The significant pair of canonical variates indicated that poor physical activity and weight control (–
of left circumflex artery stenosis 29.62 ±
0.77), poor dietary habits (–0.78), alcohol consumption and cigarette smoking (–0.37),0~100
Degree 35.74 0~100 lack of sleep
and rest (–0.40),
Degree stress
of right (–0.64)
coronary in stenosis
artery the lifestyle set,
35.05higher
± 38.62negative affectivity (0.52),
0~100 0~100 and social
inhibition (0.71) in the type-D personality
BMI = body setHDL
mass index; were= high-density
associated with a high MetS score (0.59) and
lipoprotein.
severity of CAD (.91).

(a) (b)

(c) (d)
Figure 2. Characteristics of the metabolic syndrome and the severity of coronary artery disease;
Figure 2. Characteristics of the metabolic syndrome and the severity of coronary artery disease; (a)
(a) Prevalence of metabolic syndrome components; (b) prevalence of coronary artery stenosis; (c)
Prevalence of metabolic syndrome components; (b) prevalence of coronary artery stenosis; (c) proportion
proportion of metabolic syndrome score; (d) proportion of coronary artery disease severity
of metabolic syndrome score; (d) proportion of coronary artery disease severity

3.3. Correlation between the Behavioral-Psychological Variable Set and Predictors of CAD Prognosis
Assumption tests were conducted before the canonical correlation analysis. The normality,
the linearity, and the homoscedasticity met the assumptions, except for MetS components and the
degree of stenosis in each artery. The correlation between behavioral-psychological variables and
predictors of CAD prognosis was between 0.20~0.42, which showed an absence of multicollinearity
(Table 3).
Int. J. Environ. Res. Public Health 2020, 17, 1608 8 of 14

The behavioral-psychological variable set was related to the predictor set of CAD prognosis
with one significant canonical variate of 0.67 (45% overlapping variance) (Table 4). Wilk’s Lambda
value with all canonical correlations was 0.51, which was statistically significant (F = 4.91, p < 0.001).
The significant pair of canonical variates indicated that poor physical activity and weight control
(−0.77), poor dietary habits (−0.78), alcohol consumption and cigarette smoking (−0.37), lack of sleep
and rest (−0.40), stress (−0.64) in the lifestyle set, higher negative affectivity (0.52), and social inhibition
(0.71) in the type-D personality set were associated with a high MetS score (0.59) and severity of
CAD (0.91).

Table 3. Correlation between behavioral-psychological variables and predictors for CAD prognosis.

Type-D MetS
Lifestyle
Variables Personality Score
1 2 3 4 5 6 7 8 9
1. Physical activity and weight
1
control
2. Dietary habit 0.60 *** 1
3. Drinking and smoking 0.29 ** 0.52 *** 1
4. Sleep and rest 0.44 *** 0.64 *** 0.50 *** 1
5. Stress 0.66 *** 0.65 *** 0.45 *** 0.55 *** 1
6. Drug and health management 0.08 0.37 *** 0.35 *** 0.33 *** 0.20 * 1
7. Negative affectivity −0.42 *** −0.21 * −0.06 −0.20 * −0.30 ** 0.10 1
8. Social inhibition −0.41 *** −0.23 * −0.13 −0.16 −0.25 * 0.04 0.76 *** 1
9. MetS score −0.22 * −0.22 * −0.10 0.08 −0.16 0.12 0.31 ** 0.39 ** 1
10. Severity of coronary artery
−0.51 *** −0.53 *** −0.25 ** −0.29** −0.44 *** −0.10 0.27 ** 0.38 *** 0.21 *
disease
* <0.05, ** <0.01, *** <0.001.

Table 4. Canonical correlation between behavioral-psychological variables and predictors of CAD prognosis.

Variables Canonical Variate

Set 1: Behavioral-psychological variables
Lifestyle (behavioral variables)
Physical activity and weight control −0.77
Dietary habit −0.78
Drinking and smoking −0.37
Sleep and rest −0.40
Stress −0.64
Drug and health management −0.05
Type-D personality (psychological variables)
Negative affectivity 0.52
Social inhibition 0.71
Percent of redundancies 15.14
Set 2: Predictors for CAD prognosis
Metabolic syndrome score 0.59
Severity of coronary artery disease 0.91
Percent of redundancies 26.57
Canonical correlation 0.67
Significance test; F(p) 4.91(<0.001)
Variance explained 45.0%
Int. J. Environ. Res. Public Health 2020, 17, 1608 9 of 14

4. Discussion
Participants who were older, those with acute coronary syndrome, and those with antihypertensive
medication use showed a high severity of CAD, however, there was no difference between the sexes
in terms of severity of CAD. Compared to age-matched males, premenopausal females have been
reported to have a reduced incidence of cardiovascular disease that presented 10 years later than
that in men [37] owing to the protective role of estrogen [38], however, a greater number of elderly
women were included in this study. Acute coronary syndrome has been reported to have a higher
severity of CAD than stable angina. One epidemiological study showed that mortality rates for each
acute coronary syndrome (unstable angina pectoris, STEMI, and NSTEMI) were relatively high in
the five years after diagnosis (19%, 22%, and 17%, respectively) [39]. Therefore, it is essential that
patients with acute coronary syndrome follow stringent risk management to prevent secondary events
or death. The use of antihypertensive medication was associated with a higher severity of CAD in
this study. Because of the cross-sectional study design, it was not clear whether participants had
hypertension and CAD or whether they were participants with hypertension at a high risk for CAD.
According to a follow-up study of cardiovascular disease, only 2.1% of the patients had uncontrolled
hypertension [40]. A multi-drug blood pressure control strategy that includes angiotensin-converting
enzyme inhibition in high-risk patients with CAD has been shown to be beneficial in reducing the
risk of CAD [41]. Therefore, more detailed information, including that of the type of medication and
dosage, is needed to clarify the relationship between antihypertensive medication and the severity
of CAD.
In this study, hypertriglyceridemia was the lowest component of MetS (38.9%), and the mean
MetS score was 2.92, which was consistent with trends in the prevalence of MetS as identified in
the Korean National Health Insurance Service data [42]. However, the mean triglyceride level was
134.78 mg/dL, which has been defined as a high-normal triglycerides level. In a recent cohort study,
there was an elevated risk for death in patients with high-normal triglyceride levels of 100 to 149
mg/dL compared with that in those with lower triglyceride levels [43]. Hypertriglyceridemia had the
highest hazard ratios for atheroma progression and the strongest relationship with the prevalence of
myocardial infarction and stroke in patients [44]. For patients with cardiovascular disease, regardless
of adjustment for HDL-C, elevated triglyceride levels have been associated with an increased risk
of all-cause mortality [43]. Triglyceride levels should be managed with greater vigilance. Moreover,
accelerated cardiovascular disease progression has been reported to be due to the presence of individual
components rather than due to MetS alone [45,46], and care needs to be exercised when using the
MetS score with respect to the component management of patients without MetS but who have one or
two components.
Participants had significant stenosis in 1.25 vessels on average. Similar to a previous study [15],
39.8% of participants had significant stenosis in a single coronary artery, mostly the LAD. Given
that the left ventricle end-diastolic diameter has been found to be inversely related to impaired
function in the neuropsychological phase [47], attention should be paid to the severity of LAD
stenosis. Endothelial dysfunction induces coronary abnormalities that are critical in cardiovascular
stenosis because endothelial cells regulate vascular and inflammatory responses [2]. Specifically,
type-D personality is associated with impaired endothelial dysfunction in patients with CAD [48].
The mechanism underlying the influence of type-D personality on endothelial dysfunction remains
unclear. However, type-D personality characterized by stress may be considered to indicate a high risk
because stress is known to induce endothelial dysfunction [48].
Only one pair of canonical variates was significant. The strongest variable combinations were
poor physical activity/weight control, unhealthy dietary habits, and social inhibition. A previous study
found that people with type-D personalities have less healthy lifestyles involving less physical activity
and a less varied diet [31]. A type-D personality is an independent predictor of decreased exercise
capacity and decreased motivation for activity [13]. Social inhibition is associated with interpretation
biases toward cognitive, affective, and behavioral factors [49], which may make it difficult to motivate
Int. J. Environ. Res. Public Health 2020, 17, 1608 10 of 14

patients with depression to modify their behavior. Specifically, due to traits with regard to higher
levels of anxiety and depressive mood, social inhibition plays a key role in the higher drop-out rate
from cardiac rehabilitation programs [50], and this could be also a potential cause of CAD recurrence.
Furthermore, type-D personality has been associated with significantly less healthy food intake,
including a greater consumption of fat and sugar compared with fruit and vegetable intake [16].
Patients with higher social inhibition have poor dietary habits because they often are non-adherent to
recurrence preventive regimens [14]. Saturated fat and sugar can raise total cholesterol levels in the
blood, and sugar intake can have unfavorable effects on triglyceride levels [51]. High sugar intake also
promotes insulin resistance, which is reported to be one of the main causes of CAD development due
to MetS [52]. Therefore, the combination of unhealthy physical activity/dietary habits as behavioral
components and social inhibition as the psychological component should be separately identified and
addressed to improve the prognosis for patients with CAD.
A combination of severe stress and negative affectivity has also been found to be related to a poor
CAD prognosis. Negative affectivity appears to be a significant component for mental distress [13],
and high negative affectivity has been characterized as experiencing enhanced feelings of dysphoria,
anxiety, and irritability and a negative feeling towards oneself [22]. Individuals with negative affectivity
are likely to be more focused on emotions, and, at the time of stress, cortisol is released as an effector
hormone, which influences target organs such as the heart [23], leading to increased inflammation,
which plays a critical role in the development of atherosclerosis [53]. As a result, responding emotionally
to stressful situations may worsen the CAD prognosis. Therefore, negative affectivity should be
controlled so that it does not become associated with higher stress and enhances the likelihood of a
poor CAD prognosis.
Based on our findings, a rehabilitation program that aims to prevent a combination of behavioral
and psychological variables is likely to be more effective in improving CAD prognosis and should
involve periodic type-D personality screening. In one study, a type-D personality diagnosis was found to
have altered almost 60% of patients postoperatively [54]; therefore, appropriate interventions for patients
with type-D personalities should be provided. Considering the strong relationship between unhealthy
behaviors, social inhibition, and predictors for CAD prognosis, a weaning strategy concerning social
inhibition needs to be prioritized for the rehabilitation program. Furthermore, based on the multifaceted
model of social inhibition [49], integrative intervention, such as psychodynamic intervention, should be
included to reduce cognitive, affective, and behavioral inhibition [55]. Psychodynamic intervention is
a supporting strategy for promoting self-management behavior by improving a patient’s cognitive and
affective inhibition [55]. Psychodynamic motivation and training programs have shown that improving
physical activity after myocardial infarction [56], and a stepwise psychotherapy intervention, including
group psychotherapy and incorporating cognitive-behavioral elements, can improve symptoms of
depression in patients with CAD [57].

5. Limitation
This study has several limitations. First, the data were derived from a single cardiology center using
a convenience sampling method; therefore, some results of this study may not be generalizable to all
Koreans. Thus, future studies should include a greater number of participants and clinics. Second, we
could not define the causal relationship between behavioral-psychological change and CAD prognosis
because our study was not longitudinal. Therefore, longitudinal screening for behavioral-psychological
factors is required when designing future studies. Third, bias may have occurred when evaluating
disease-related participant characteristic data extracted from medical records, and recall bias may have
occurred when information was obtained from survey responses. Thus, a prospective study design
may be merited to eliminate potential bias. Finally, participants’ use of antihyperlipidemic medication
was not classified in terms of antitriglyceride and anticholesterol medication because these data were
recorded in the outpatient department and not in the medical records. Therefore, participants using
antihyperlipidemic medication may have been unnecessarily checked for hypertriglyceridemia and
Int. J. Environ. Res. Public Health 2020, 17, 1608 11 of 14

low HDL-C components, and an over-estimation may have been possible when calculating the MetS
score. Therefore, these results should be interpreted cautiously.

6. Conclusions
Pairs of behavioral-psychological variables, specifically a combination of physical activity/weight
control, dietary habits, and social inhibition, were found to be predictors of CAD prognosis. As several
behavioral factors might be controlled through identification as subcategories of type-D personality,
the combination of behavior-psychological factors should be separately identified and addressed to
improve the prognosis of patients with CAD. Therefore, when preparing a rehabilitation program,
combination-separating strategies for behavior-psychological factors are likely to be more effective in
enhancing prognosis for CAD.

Author Contributions: Conceptualization, I.-K.N., J.M.R., E.J.B., H.J.C. and M.S.K.; Methodology, Formal Analysis,
M.S.K. and I.-K.N.; Data curation, J.M.R., E.J.B., H.J.C. and M.S.K.; Writing-Original Draft Preparation, J.M.R.,
E.J.B., H.J.C., M.S.K. and C.-H.K.; Writing-Review and Editing, M.S.K. and C.-H.K. All authors have read and
agreed to the published version of the manuscript.
Funding: This work was supported by the Dong-A University research fund.
Acknowledgments: The authors disclose receipt of the following financial support for the research, authorship,
and/or publication of this article.
Conflicts of Interest: The authors declare no conflict of interest.

References
1. Kolovou, G.; Kolovou, V.; Koutelou, M.; Mavrogeni, S. Atherosclerotic and non-atherosclerotic coronary
heart disease in women. Curr. Med. Chem. 2015, 22, 3555–3564. [CrossRef] [PubMed]
2. Shimokawa, H. 2014 Williams Harvey Lecture: Importance of coronary vasomotion abnormalities-from
bench to bedside. Eur. Heart J. 2014, 35, 3180–3193. [CrossRef]
3. Gheorghe, A.; Griffiths, U.; Murphy, A.; Legido-Quigley, H.; Lamptey, P.; Perel, P. The economic burden
of cardiovascular disease and hypertension in low- and middle-income countries: A systematic review.
BMC Public Health 2018, 18, 975. [CrossRef] [PubMed]
4. Bauters, C.; Deneve, M.; Tricot, O.; Meurice, T.; Lamblin, N.; CORONOR Investigators. Prognosis of patients
with stable coronary artery disease (from the CORONOR study). Am. J. Cardiol. 2014, 113, 1142–1145.
[CrossRef] [PubMed]
5. Severino, P.; D’Amato, A.; Netti, L.; Pucci, M.; De Marchis, M.; Palmirotta, R.; Volterrani, M.; Mancone, M.;
Femele, F. Diabetes mellitus and ischemic heart disease: The role of ion channels. Int. J. Mol. Sci. 2018, 19,
802. [CrossRef] [PubMed]
6. Severino, P.; Mariani, M.V.; Maraone, A.; Piro, A.; Ceccacci, A.; Tarsitani, L.; Maestrini, V.; Mancone, M.;
Lavalle, C.; Pasquini, M.; et al. Triggers for atrial fibrillation: The role of anxiety. Cardiol. Res. Pract. 2019,
2019, 1208505. [CrossRef]
7. Tune, J.D.; Goodwill, A.G.; Sassoon, D.J.; Mather, K.J. Cardiovascular consequences of metabolic syndrome.
Transl. Res. 2017, 183, 57–70. [CrossRef]
8. Kim, I.; Kim, M.C.; Sim, D.S.; Hong, Y.J.; Kim, J.H.; Jeong, M.H.; Cho, J.G.; Park, J.C.; Seung, K.B.; Chang, K.;
et al. Effect of the metabolic syndrome on outcomes in patients aged 50 years with acute myocardial infarction.
Am. J. Cardiol. 2018, 122, 192–198. [CrossRef]
9. Pelliccia, F.; Pasceri, V.; Niccoli, G.; Tanzilli, G.; Speciale, G.; Gaudio, C.; Crea, F.; Camici, P.G. Predictors
of mortality in myocardial infarction and nonobstructed coronary arteries: A systematic review and
meta-regression. Am. J. Med. 2020, 133, 73–83.e4. [CrossRef]
10. Lee, J.M.; Choi, K.H.; Koo, B.K.; Park, J.; Kim, J.; Hwang, D.; Rhee, T.M.; Kim, H.Y.; Jung, H.W.; Kim, K.J.;
et al. Prognostic implications of plaque characteristics and stenosis severity patients with coronary artery
disease. J. Am. Coll. Cardiol. 2019, 73, 2413–2424. [CrossRef]
11. Svansdottir, E.; Denollet, J.; Thorsson, B.; Gudnason, T.; Halldorsdottir, S.; Gudnason, V.; van den Broek, K.C.;
Karlsson, H.D. Association of type D personality with unhealthy lifestyle, and estimated risk of coronary
events in the general Icelandic population. Eur. J. Prev. Cardiol. 2013, 20, 322–330. [CrossRef]
Int. J. Environ. Res. Public Health 2020, 17, 1608 12 of 14

12. Varghese, T.; Schultz, W.M.; McCue, A.A.; Lambert, C.T.; Sandesara, P.B.; Eapen, D.J.; Gordon, N.F.;
Franklin, B.A.; Sperling, L.S. Physical activity in the prevention of coronary heart disease: Implications for
the clinician. Heart 2016, 102, 904–909. [CrossRef]
13. Bunevicius, A.; Brozaitiene, J.; Staniute, M.; Gelziniene, V.; Duoneliene, I.; Pop, V.J.; Bunevicius, R.; Denollet, J.
Decreased physical effort, fatigue, and mental distress in patients with coronary artery disease: Importance
of personality-related differences. Int. J. Behav. Med. 2014, 21, 240–247. [CrossRef]
14. Patterson, R.; McNamara, E.; Tainio, M.; de Sa, T.H.; Smith, A.D.; Sharp, S.J.; Edwards, P.; Woodcock, J.;
Brage, S.; Wijndaele, K. Sedentary behaviour and risk of all-cause, cardiovascular and cancer mortality, and
incident type 2 diabetes: A systematic review and dose response meta-analysis. Eur. J. Epidemiol. 2018, 33,
811–829. [CrossRef]
15. Maroszynska-Dmoch, E.M.; Wozakowska-Kaplon, B. Clinical and angiographic characteristics of coronary
artery disease in young adults: A single centre study. Kardiol. Pol. 2016, 74, 314–321. [CrossRef]
16. Booth, L.; Williams, L. Type D personality and dietary intake: The mediating effects of coping style. J. Health
Psychol. 2015, 20, 921–927. [CrossRef]
17. Kim, J.H.; Hayek, S.S.; Ko, Y.A.; Liu, C.; Samman Tahhan, A.; Ali, S.; Alkhoder, A.; Gafeer, M.M.; Choudhary, F.;
Bhimani, R.; et al. Sleep duration and mortality in patients with coronary artery disease. Am. J. Cardiol. 2019,
123, 874–881. [CrossRef]
18. Smaardijk, V.R.; Lodder, P.; Kop, W.J.; van Gennep, B.; Maas, A.H.E.M.; Mommersteeg, P.M.C. Sex- and
gender-stratified risks of psychological factors for incident ischemic heart disease: Systematic review and
meta-analysis. J. Am. Heart Assoc. 2019, 8, e010859. [CrossRef]
19. Cohen, B.E.; Edmondson, D.; Kronish, I.M. State of the art review: Depression, stress, anxiety, and
cardiovascular disease. Am. J. Hypertens. 2015, 28, 1295–1302. [CrossRef]
20. Yusuf, S.; Hawken, S.; Ounpuu, S.; Dans, T.; Avezum, A.; Lanas, F.; McQueen, M.; Budaj, A.; Pais, P.; Varigos, J.
INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial
infarction in 52 countries (the INTERHEART study): Case-control study. Lancet 2004, 364, 937–952. [CrossRef]
21. Newhouse, A.; Jiang, W. Heart failure and depression. Heart Fail Clin. 2014, 10, 295–304. [CrossRef]
22. Denollet, J. DS14: Standard assessment of negative affectivity, social inhibition, and Type D personality.
Psychosom. Med. 2005, 67, 89–97. [CrossRef]
23. Pedersen, S.S.; Denollet, J. Is type D personality here to stay? Emerging evidence across cardiovascular
disease patient groups. Curr. Cardiol. Rev. 2006, 2, 205–213. [CrossRef]
24. Whitehead, D.L.; Perkins-Porras, L.; Strike, P.C.; Magid, K.; Steptoe, A. Cortisol awakening response is
elevated in acute coronary syndrome patients with type-D personality. J. Psychosom. Res. 2007, 62, 419–425.
[CrossRef]
25. Hausteiner, C.; Klupsch, D.; Emeny, R.; Baumert, J.; Ladwig, K.H.; KORA Investigators. Clustering of negative
affectivity and social inhibition in the community: Prevalence of type D personality as a cardiovascular risk
marker. Psychosom. Med. 2010, 72, 163–171. [CrossRef]
26. Williams, L.; O’Connor, R.C.; Howard, S.; Hughes, B.M.; Johnston, D.W.; Hay, J.L.; O’Connor, D.B.; Lewis, C.A.;
Ferguson, E.; Sheehy, N.; et al. Type-D personality mechanisms of effect: The role of health-related behavior
and social support. J. Psychosom. Res. 2008, 64, 63–69. [CrossRef]
27. Leu, H.B.; Yin, W.H.; Tseng, W.K.; Wu, Y.W.; Lin, T.H.; Yeh, H.I.; Cheng Chang, K.; Wang, J.H.; Wu, C.C.;
Chen, J.W. Impact of type D personality on clinical outcomes in asian patients with stable coronary artery
disease. J. Formos. Med. Assoc. 2019, 18, 721–729.
28. Carney, C.E.; Edinger, J.D.; Kuchibhatla, M.; Lachowski, A.M.; Bogouslavsky, O.; Krystal, A.D.; Shapiro, C.M.
Cognitive behavioral insomnia therapy for those with insomnia and depression: A randomized controlled
clinical trial. Sleep 2017, 40, 1–13. [CrossRef]
29. Kupper, N.; Denollet, J. Type D Personality as a risk factor in coronary heart disease: A review of current
evidence. Curr. Cardiol. Rep. 2018, 20, 104. [CrossRef]
30. Kelpis, T.G.; Anastasiadis, K.; Nimatoudis, I.; Kelpi, M.G.; Hadjimiltiades, S.; Papakonstantinou, C. Prevalence
of “distressed” personality in patients with coronary artery disease and its correlation with morbidity after
coronary surgery. Hell. J. Cardiol. 2013, 54, 362–367.
31. Gilmour, J.; Williams, L. Type D personality is associated with maladaptive health-related behaviours.
J. Health Psychol. 2012, 17, 471–478. [CrossRef]
Int. J. Environ. Res. Public Health 2020, 17, 1608 13 of 14

32. Tabachnick, B.G.; Fidell, L.S. Using Multivariate Statistics, 4th ed.; Allyn & Bacon: Boston, MA, USA,
2013; p. 199.
33. Kang, S.W. The validity and reliability of a lifestyle evaluation tool for patients with metabolic syndrome.
J. Korean Acad. Fund. Nurs. 2010, 17, 487–497. [CrossRef]
34. Lim, H.E.; Lee, M.S.; Ko, Y.H.; Park, Y.M.; Joe, S.H.; Kim, Y.K.; Han, C.; Lee, H.Y.; Pedersen, S.S.; Denollet, J.
Assessment of the type D personality construct in the Korean population: A validation study of the Korean
DS14. J. Korean Med. Sci. 2011, 26, 116–123. [CrossRef]
35. Grundy, S.M.; Cleeman, J.I.; Daniels, S.R.; Donato, K.A.; Eckel, R.H.; Franklin, B.A.; Gordon, D.J.; Krauss, R.M.;
Savage, P.J.; Smith, S.C.; et al. Diagnosis and management of the metabolic syndrome: An American
heart Association/National heart, lung, and blood institute scientific statement: Executive summary.
Crit. Pathw. Cardiol. 2005, 4, 198–203.
36. Shin, H.M.; Jee, S.H.; Kim, J.H.; Kim, M.R. The influence on cadiovascular mortality of the metabolic
syndrome in Korean post-menopause women. J. Korean Soc. Menopause 2012, 18, 6–14. [CrossRef]
37. Wake, R.; Yoshiyama, M. Gender differences in ischemic heart disease. Recent Pat. Cardiovasc. Drug. Discov.
2009, 4, 234–240. [CrossRef]
38. Iorga, A.; Cunningham, C.M.; Moazeni, S.; Ruffenach, G.; Umar, S.; Eqhbali, M. The protective role of
estrogen and estrogen receptors in cardiovascular disease and the controversial use of estrogen therapy.
Biol. Sex Differ. 2017, 8, 33. [CrossRef]
39. Fox, K.A.; Carruthers, K.F.; Dunbar, D.R.; Graham, C.; Manning, J.R.; De Raedt, H.; Buysschaert, I.;
Lambrechts, D.; Van de Werf, F. Underestimated and under-recognized: The late consequences of acute
coronary syndrome (GRACE UK–Belgian Study). Eur. Heart J. 2010, 31, 2755–2764. [CrossRef]
40. Schoenenberger, A.W.; Jamshidi, P.; Kobza, R.; Zuber, M.; Stuck, A.E.; Pfisterer, M.; Erne, P. Progression of
coronary artery disease during long-term follow-up of the Swiss Interventional Study on Silent Ischemia
Type II (SWISSI II). Clin. Cardiol. 2010, 3, 289–295. [CrossRef]
41. Pepine, C.J.; Kowey, P.R.; Kupfer, S.; Kolloch, R.E.; Benetos, A.; Mancia, G.; Coca, A.; Cooper-DeHoff, R.M.;
Handberg, E.; Gaxiola, E.; et al. Predictors of adverse outcome among patients with hypertension and
coronary artery disease. J. Am. Coll. Cardiol. 2006, 47, 547–551.
42. Lee, S.E.; Han, K.; Kang, Y.M.; Kim, S.O.; Cho, Y.K.; Ko, K.S.; Park, J.Y.; Lee, K.U.; Koh, E.H.; Taskforce Team
of Diabetes Fact Sheet of the Korean Diabetes Association. Trends in the prevalence of metabolic syndrome
and its components in south Korea: Findings from the Korean national health insurance service database
(2009–2013). PLoS ONE 2018, 13, e0194490. [CrossRef] [PubMed]
43. Klempfner, R.; Erez, A.; Sagit, B.Z.; Goldenberg, I.; Fisman, E.; Kopel, E.; Shlomo, N.; Israel, A.; Tenenbaum, A.
Elevated triglyceride level is independently associated with increased all-cause mortality in patients with
established coronary heart disease: Twenty-two-year follow-up of the bezafibrate infarction prevention
study and registry. Circ. Cardiovasc. Qual. Outcomes 2016, 9, 100–108. [CrossRef] [PubMed]
44. Bayturan, O.; Tuzcu, E.M.; Lavoie, A.; Hu, T.; Wolski, K.; Schoenhagen, P.; Schoenhagen, P.; Kapadia, S.;
Nissen, S.E.; Nicholls, S.J. The metabolic syndrome, its component risk factors, and progression of coronary
atherosclerosis. Arch. Intern. Med. 2010, 170, 478–484. [CrossRef] [PubMed]
45. Gui, M.H.; Ling, Y.; Liu, L.; Jiang, J.J.; Li, X.Y.; Gao, X. Effect of metabolic syndrome score, metabolic
syndrome, and its individual components on the prevalence and severity of angiographic coronary artery
disease. Chin. Med. J. (Engl) 2017, 130, 669–677. [CrossRef]
46. Wiley, J.F.; Carrington, M.J. A metabolic syndrome severity score: A tool to quantify cardio-metabolic risk
factors. Prev. Med. 2016, 88, 189–195. [CrossRef]
47. Carbonara, R.; Giardinelli, F.; Zito, A.; Scicchitano, P.; Dentamaro, I.; Cortese, F.; Armenise, A.; Manca, F.;
De Caro, M.F.; Nazzaro, P.; et al. Neuro-Psychological Pattern in Patients Suffering from Primitive Dilated
Cardiomyopathy with Impairment in Executive Function. Curr. Neurovasc. Res. 2017, 14, 39–45. [CrossRef]
48. Denollet, J.; van Felius, R.A.; Lodder, P.; Mommersteeg, P.M.; Goovaerts, I.; Possemiers, N.; Vanhees, L.;
Beckers, N.; Pattyn, N.; Van Craenenbroeck, E.M. Predictive value of Type D personality for impaired
endothelial function in patients with coronary artery disease. Int. J. Cardiol. 2018, 259, 205–210. [CrossRef]
49. Denollet, J.; Pedersen, S.S.; Vrints, C.J.; Conraads, V.M. Predictive value of social inhibition and negative
affectivity for cardiovascular events and mortality in patients with coronary artery disease: The type D
personality construct. Psychosom. Med. 2013, 75, 873–881. [CrossRef]
Int. J. Environ. Res. Public Health 2020, 17, 1608 14 of 14

50. Lee, S.J.; Koh, S.; Kim, B.O.; Kim, B.; Kim, C. Effect of type D Personality on short-term cardiac rehabilitation
in patients with coronary artery disease. Ann. Rehabil. Med. 2018, 42, 748–757. [CrossRef]
51. DiNicolantonio, J.J.; Lucan, S.C.; O’Keefe, J.H. The evidence for saturated fat and for sugar related to coronary
heart disease. Prog. Cardiovasc. Dis. 2016, 58, 464–472. [CrossRef]
52. Ormazabal, V.; Nair, S.; Elfeky, O.; Aguayo, C.; Salomon, C.; Zuniga, F.A. Association between insulin
resistance and the development of cardiovascular disease. Cardiovasc. Diabetol. 2018, 17, 122. [CrossRef]
53. Yao, B.C.; Meng, L.B.; Hao, M.L.; Zhang, Y.M.; Gong, T.; Guo, Z.G. Chronic stress: A critical risk factor for
atherosclerosis. J. Int. Med. Res. 2019, 47, 1429–1440. [CrossRef]
54. Dannemann, S.; Matschke, K.; Einsle, F.; Smucker, M.R.; Zimmermann, K.; Joraschky, P.; Weidner, K.;
Kollner, V. Is type-D a stable construct? An examination of type-D personality in patients before and after
cardiac surgery. J. Psychosom. Res. 2010, 69, 101–109. [CrossRef]
55. Venuleo, C.; Mangeli, G.; Mossi, P.; Amico, A.F.; Cozzolino, M.; Distante, A.; Ignone, G.; Savarese, G.;
Salvatore, S. The cardiac rehabilitation psychodynamic group intervention (CR-PGI): An explorative study.
Front. Psychol. 2018, 9, 976. [CrossRef]
56. Michal, M.; Simon, P.; Gori, T.; Konig, J.; Wild, P.S.; Wiltink, J.; Tug, S.; Sterzing, B.; Unterrrainer, J.; Munzel, T.;
et al. Psychodynamic Motivation and Training program (PMT) for the secondary prevention in patients
with stable coronary heart disease: Study protocol for a randomized controlled trial of feasibility and effects.
Trials 2013, 14, 314.
57. Albus, C.; Beutel, M.E.; Deter, H.C.; Fritzsche, K.; Hellmich, M.; Jordan, J.; Juenger, J.; Krauth, C.; Ladwig, K.H.;
Michal, M.; et al. A stepwise psychotherapy intervention for reducing risk in coronary artery disease
(SPIRR-CAD)—rationale and design of a multicenter, randomized trial in depressed patients with CAD.
J. Psychosom. Res. 2011, 71, 215–222. [CrossRef]

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access
article distributed under the terms and conditions of the Creative Commons Attribution
(CC BY) license (http://creativecommons.org/licenses/by/4.0/).